Developmental plasticity

About: Developmental plasticity is a research topic. Over the lifetime, 1721 publications have been published within this topic receiving 103438 citations.

Synaptic plasticity, neural circuits, and the emerging role of altered short-term information processing in schizophrenia

Abstract: Synaptic plasticity alters the strength of information flow between presynaptic and postsynaptic neurons and thus modifies the likelihood that action potentials in a presynaptic neuron will lead to an action potential in a postsynaptic neuron. As such, synaptic plasticity and pathological changes in synaptic plasticity impact the synaptic computation which controls the information flow through the neural microcircuits responsible for the complex information processing necessary to drive adaptive behaviors. As current theories of neuropsychiatric disease suggest that distinct dysfunctions in neural circuit performance may critically underlie the unique symptoms of these diseases, pathological alterations in synaptic plasticity mechanisms may be fundamental to the disease process. Here we consider mechanisms of both short-term and long-term plasticity of synaptic transmission and their possible roles in information processing by neural microcircuits in both health and disease. As paradigms of neuropsychiatric diseases with strongly implicated risk genes, we discuss the findings in schizophrenia and autism and consider the alterations in synaptic plasticity and network function observed in both human studies and genetic mouse models of these diseases. Together these studies have begun to point toward a likely dominant role of short-term synaptic plasticity alterations in schizophrenia while dysfunction in autism spectrum disorders (ASDs) may be due to a combination of both short-term and long-term synaptic plasticity alterations.

Toward a theory of neuroplasticity

Abstract: Contents: Section I: Introduction to Neuroplasticity. C.A. Shaw & J.C. McEachern, Is There a General Theory of Neuroplasticity? G.C. Teskey, A General Framework for Neuroplasticity Theories and Models. Section II: Behavioural and Systems Approaches to Experience, Learning and Memory. W.M. DeBello & E.I. Knudsen, Adaptive Plasticity of the Auditory Space Map. N.M. Weinberger, Learning and Receptive Field Plasticity in Auditory Cortex: Identification of a Memory Code? Y. Sugita, Global Plasticity of the Adult Visual System, J.L. Kavanau, Reinforcement of Memory During Sleep. A.R. Mercer, The Predictable Plasticity of Honey Bees. Section III: Circuit, Cellular and Synaptic Aspects of Neuroplasticity. B.K. Ormerod & L.A.M. Galea, Mechanism and Function of Adult Neurogenesis. T. J. Teyler, LTP and the Superfamily of Synaptic Plasticities. D. P. Cain, Synaptic Models of Neuroplasticity: What is LTP? N.S. Desai, S.B. Nelson & G.G. Turrigiano, Homeostatic Regulation of Cortical Networks. Section IV: Molecular and Genetic Determinants of Neuroplasticity. L. Liu & Y. T. Wang, Regulation of Postsynaptic Receptor Trafficking - A Novel Means of Generating Synaptic Plasticity. G.D. Mower, Immediate Early Gene Expression and Critical Period Neuroplasticity in Visual Cortex. J.K. Rose & C.H. Rankin, Behavioral, Neural Circuit and Genetic Analyses of Habituation in C. elegans. M. Saitoe & T. Tully, Making Connections Between Developmental and Behavioral Plasticity in Drosophila. Section V: Developmental Aspects of Neuroplasticity. B. Kolb, R. Gibb & C.L.R. Gonzalez, Cortical Injury and Neuroplasticity During Brain Development. J. P. Rauschecker, Developmental Neuroplasticity Within and Across Sensory Modalities. H. Neville & D. Bavelier, Specificity of Developmental Neuroplasticity in Humans: Evidence from Sensory Deprivation and Altered Language Experience. H. M. Lenhoff, O. Perales & G.S. Hickok, Preservation of a Normally Transient Critical Period in a Cognitively Impaired Population: Window of Opportunity for Acquiring Absolute Pitch in Williams Syndrome. T. Bredy, I. Weaver, F.C. Champagne & M.J. Meaney, Maternal Care and Neural Development in the Rat. H. Anisman, S. Hayley, Wm. Staines & Z. Merali, Cytokines, Stress, and Neurochemical Change: Immediate and Proactive Effects. Section VI: 'Pathological' Neuroplasticity and the Response to Injury. J. H. Kaas, The Mutability of Sensory Representations After Injury in Adult Mammals. G. S. Doetsch, Phantoms and Other Perceptual Phenomena Related to Plasticity in Somatosensory Cortex. G. C. Teskey, Using Kindling to Model the Neuroplastic Changes Associated with Learning and Memory, Neuropsychiatric Disorders and Epilepsy. M. E. Wolf. The Neuroplasticity of Addiction. G. Baranauskas, Pain Induced Plasticity in Spinal Cord. D. Neill, Maladaptive and Dysfunctional Synaptoplasticity in Relation to Alzheimer's Disease and Schizophrenia. M. P. Mattson, W. Duan, S.L. Chan & Z. Guo, Apoptotic and Anti-Apoptotic Signaling at the Synapse: From Adaptive Plasticity to Neurodegenerative Disorders. Section VII: Is There a Theory of Neuroplasticity? C.A. Shaw & J.C. McEachern, Traversing Levels of Organization: A Theory of Neuronal Stability and Plasticity

A heuristic model on the role of plasticity in adaptive evolution: plasticity increases adaptation, population viability and genetic variation

Abstract: An ongoing new synthesis in evolutionary theory is expanding our view of the sources of heritable variation beyond point mutations of fixed phenotypic effects to include environmentally sensitive changes in gene regulation. This expansion of the paradigm is necessary given ample evidence for a heritable ability to alter gene expression in response to environmental cues. In consequence, single genotypes are often capable of adaptively expressing different phenotypes in different environments, i.e. are adaptively plastic. We present an individual-based heuristic model to compare the adaptive dynamics of populations composed of plastic or non-plastic genotypes under a wide range of scenarios where we modify environmental variation, mutation rate and costs of plasticity. The model shows that adaptive plasticity contributes to the maintenance of genetic variation within populations, reduces bottlenecks when facing rapid environmental changes and confers an overall faster rate of adaptation. In fluctuating environments, plasticity is favoured by selection and maintained in the population. However, if the environment stabilizes and costs of plasticity are high, plasticity is reduced by selection, leading to genetic assimilation, which could result in species diversification. More broadly, our model shows that adaptive plasticity is a common consequence of selection under environmental heterogeneity, and hence a potentially common phenomenon in nature. Thus, taking adaptive plasticity into account substantially extends our view of adaptive evolution.

Extracellular matrix in plasticity and epileptogenesis.

Abstract: Extracellular matrix (ECM) in the brain is composed of molecules synthesized and secreted by neurons and glial cells in a cell-type-specific and activity-dependent manner. During development, ECM plays crucial roles in proliferation, migration and differentiation of neural cells. In the mature brain, ECM undergoes a slow turnover and supports multiple physiological processes, while restraining structural plasticity. In the first part of this review, we discuss the contribution of ECM molecules to different forms of plasticity, including developmental plasticity in the cortex, long-term potentiation and depression in the hippocampus, homeostatic scaling of synaptic transmission and metaplasticity. In the second part, we focus on pathological changes associated with epileptogenic mutations in ECM-related molecules or caused by seizure-induced remodeling of ECM. The available data suggest that ECM components regulating physiological plasticity are also engaged in different aspects of epileptogenesis, such as dysregulation of excitatory and inhibitory neurotransmission, sprouting of mossy fibers, granule cell dispersion and gliosis. At the end, we discuss combinatorial approaches that might be used to counteract seizure-induced dysregulation of both ECM molecules and extracellular proteases. By restraining ECM modification and preserving the status quo in the brain, these treatments might prove to be valid therapeutic interventions to antagonize the progression of epileptogenesis.